ArticleThe Journal of biological chemistry2015
Krüppel-like factor 2 represses transcription of the telomerase catalytic subunit human telomerase reverse transcriptase (hTERT) in human T cells.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Persistent CD4Cellular immunology · 2026Article
- The Relevance of Telomerase and Telomere-Associated Proteins in B-Acute Lymphoblastic Leukemia.Genes · 2023Review
- Acute type adult T-cell leukemia cells proliferate in the lymph nodes rather than in peripheral blood.Cancer gene therapy · 2022Article
- Promoter CpG methylation inhibits Krüppel-like factor 2 (KLF2)-Mediated repression of hTERT gene expression in human T-cells.Biochemistry and biophysics reports · 2021Article
- Expression and regulation of telomerase in human T cell differentiation, activation, aging and diseases.Cellular immunology · 2019Review
- Discovering human transcription factor physical interactions with genetic variants, novel DNA motifs, and repetitive elements using enhanced yeast one-hybrid assays.Genome research · 2019Article
- Aging and the Krüppel-like factors.Trends in cell & molecular biology · 2017Article
- Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In normal human T cells, telomerase activity is strictly regulated. T cells are thought to express telomerase to avoid replicative senescence, unlike most normal somatic cells with definite replicative lifespan. T cells in blood and tissues are usually in a state of quiescence without expression of the limiting catalytic subunit of telomerase, human telomerase reverse transcriptase (hTERT). In contrast to activation, repression of hTERT transcription has not been studied well. Our previous studies have found an hTERT promoter element with repressive function. Here we identified KLF2, which represses hTERT transcription by binding to the putative promoter element. KLF2 and hTERT exhibited reciprocal mRNA expression patterns in primary human T cells. In activated T cells, KLF2 binding to the hTERT promoter was eliminated, relieving the repression of hTERT transcription found in resting T cells. Our results suggest that KLF2 is involved in strict repression of hTERT expression through binding to the promoter in primary human T cells.
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